J Hui1, W Huishan2, L Tao1, Y Zhonglu1, Z Renteng1, H Hongguang1. 1. Department of Cardiovascular Surgery, The General Hospital of Shenyang Military Region, No. 83Wenhua Road, 110016, Shenhe District, Shenyang, Liaoning, China. 2. Department of Cardiovascular Surgery, The General Hospital of Shenyang Military Region, No. 83Wenhua Road, 110016, Shenhe District, Shenyang, Liaoning, China. wanghuishan2016@sina.com.
Abstract
BACKGROUND: Myocardial infarction is one of the most common causes of death, and the number of individuals at risk is increasing. A rapid and accurate differential diagnosis of myocardial infarction is crucial for timely interventions and for improvement of the prognosis. However, it is difficult to achieve using current methods. To better manage this condition, improved tools for risk prediction, including more accurate biomarkers, are needed. METHODS: We studied the expression of microRNA-539 (miR-539) and of MEK protein using a rat model of myocardial infarction. RESULTS: The results of our experiments demonstrated an increase in the expression of miR-539 and a decrease in the expression of MEK. Furthermore, we observed that miR-539 inhibited the expression of MEK through targeting of the 3'UTR of MEK; this led not only to suppressed proliferation but also to apoptosis and autophagy of H9C2 cells. CONCLUSION: Overexpression of miR-539 plays a role in the degree of myocardial infarction. On the basis of our results, we conclude that miR-539 may be a potential therapeutic target for myocardial infarction.
BACKGROUND:Myocardial infarction is one of the most common causes of death, and the number of individuals at risk is increasing. A rapid and accurate differential diagnosis of myocardial infarction is crucial for timely interventions and for improvement of the prognosis. However, it is difficult to achieve using current methods. To better manage this condition, improved tools for risk prediction, including more accurate biomarkers, are needed. METHODS: We studied the expression of microRNA-539 (miR-539) and of MEK protein using a rat model of myocardial infarction. RESULTS: The results of our experiments demonstrated an increase in the expression of miR-539 and a decrease in the expression of MEK. Furthermore, we observed that miR-539 inhibited the expression of MEK through targeting of the 3'UTR of MEK; this led not only to suppressed proliferation but also to apoptosis and autophagy of H9C2 cells. CONCLUSION: Overexpression of miR-539 plays a role in the degree of myocardial infarction. On the basis of our results, we conclude that miR-539 may be a potential therapeutic target for myocardial infarction.
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